Plasma lipids increase sharply with the onset of suckling in the neonatal rat. Much of the variation has been attributed to the high fat content of milk. Apoproteins AI, E and AIV were found in low concentrations in the fetus. They increased during suckling. Apoprotein E and apoprotein AIV did not exceed adult values whereas apoprotein AI concentration in the late suckling period was twice that of the adult. On the contrast, fetal apoprotein B was nearly 2.5-fold above adult concentration and was under the form of LDL, the main lipoprotein class in the late fetal period. Apoprotein B concentration decreased progressively as LDL was replaced by an apoprotein E-rich HDL. The latter class constituted an important transitory cholesterol carrier during the shift from the neonatal lipoprotein pattern dominated by LDL to the typical adult pattern in which HDL are predominant. Lack of active cholesterol ester transfer protein is believed to be one of the reasons for low LDL concentration in adult rats. However, in vitro incubation of radioactively-labelled HDL cholesteryl esters with rat plasma demonstrated that the juveniles' lipoprotein depleted plasma induced as little transfer of the label from HDL to lower density lipoproteins as that of the adult. Thus a transient cholesteryl ester transfer activity could not have contributed to the composition of the LDL pool in the fetus and the early suckling rat. It is more likely that LDL are secreted directly by the liver. Each apolipoprotein exhibited a characteristic developmental pattern different from that of adult rats fed hyperlipidic diets. It therefore appears that each apoprotein is controlled independently by a combination of programmed ontogenic development and nutritional factors leading to the progressive establishment of the adult lipoprotein profile.